We have demonstrated that TLK1 can promote androgen-dependent to androgen-independent progression and survival of PCa cells through various mechanisms, such as hyperactivating NEK1 and NEK1-mediated activation of ATR > Chk1 or VDAC1, stabilization of YAP1, or by directly regulating AKT through AKTIP phosphorylation [13,14,15,16,17,18]. This evidence concerns the gene TLK1 and posterior cortical atrophy.